Critical Reviews in Microbiology最新文献

The oral microbiome, populated by a diverse range of species, plays a critical role in the initiation and progression of periodontal disease. The most dominant yet little-discussed players in the microbiome, the bacteriophages, influence the health and disease of the host in various ways. They, not only contribute to periodontal health by preventing the colonization of pathogens and disrupting biofilms but also play a role in periodontal disease by upregulating the virulence of periodontal pathogens through the transfer of antibiotic resistance and virulence factors. Since bacteriophages selectively infect only bacterial cells, they have an enormous scope to be used as a therapeutic strategy; recently, phage therapy has been successfully used to treat antibiotic-resistant systemic infections. Their ability to disrupt biofilms widens the scope against periodontal pathogens and dental plaque biofilms in periodontitis. Future research focussing on the oral phageome and phage therapy's effectiveness and safety could pave way for new avenues in periodontal therapy. This review explores our current understanding of bacteriophages, their interactions in the oral microbiome, and their therapeutic potential in periodontal disease.

In this review, we address the interplay between the complement system and host microbiomes in health and disease, focussing on oral bacteria known to contribute to homeostasis or to promote dysbiosis associated with dental caries and periodontal diseases. Host proteins modulating complement activities in the oral environment and expression profiles of complement proteins in oral tissues were described. In addition, we highlight a sub-set of bacterial proteins involved in complement evasion and/or dysregulation previously characterized in pathogenic species (or strains), but further conserved among prototypical commensal species of the oral microbiome. Potential roles of these proteins in host-microbiome homeostasis and in the emergence of commensal strain lineages with increased virulence were also addressed. Finally, we provide examples of how commensal bacteria might exploit the complement system in competitive or cooperative interactions within the complex microbial communities of oral biofilms. These issues highlight the need for studies investigating the effects of the complement system on bacterial behaviour and competitiveness during their complex interactions within oral and extra-oral host sites.

The cause of Alzheimer's disease (AD), and the pathophysiological mechanisms involved, remain major unanswered questions in medical science. Oral bacteria, especially those species associated with chronic periodontitis and particularly Porphyromonas gingivalis, are being linked causally to AD pathophysiology in a subpopulation of susceptible individuals. P. gingivalis produces large amounts of proteolytic enzymes, haem and iron capture proteins, adhesins and internalins that are secreted and attached to the cell surface and concentrated onto outer membrane vesicles (OMVs). These enzymes and adhesive proteins have been shown to cause host tissue damage and stimulate inflammatory responses. The ecological and pathophysiological roles of P. gingivalis OMVs, their ability to disperse widely throughout the host and deliver functional proteins lead to the proposal that they may be the link between a P. gingivalis focal infection in the subgingivae during periodontitis and neurodegeneration in AD. P. gingivalis OMVs can cross the blood brain barrier and may accelerate AD-specific neuropathology by increasing neuroinflammation, plaque/tangle formation and dysregulation of iron homeostasis, thereby inducing ferroptosis leading to neuronal death and neurodegeneration.

Although the importance of deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) sensors in controlling viral infection is well established, their role in promoting an effective immune response to pathogens other than viruses is less clear. This is particularly true for infections with mycobacteria, as studies point to both protective and detrimental roles for activation of nucleic acid sensors in controlling a mycobacterial infection. Some of the contradiction likely stems from the use of different model systems and different mycobacterial species/strains as well as from which nucleic acid sensors were studied and what downstream effectors were evaluated. In this review, we will describe the different nucleic acid sensors that have been studied in the context of mycobacterial infections, and how the different studies compare. We conclude with a section on how nucleic acid sensor agonists have been used therapeutically and what further information is needed to enhance their potential as therapeutic agents.

The opportunistic human pathogen Pseudomonas aeruginosa can cause severe infections in immunocompromized people or cystic fibrosis (CF) patients. Because of its remarkable ability to invade the host and withstand the bacteriocidal effect of most conventional antibiotics, the infection caused by P. aeruginosa has become a major concern for human health. The switch from acute to chronic infection is governed by the second messenger bis-(3'-5')-cyclic dimeric guanosine mono-phosphate (c-di-GMP) in P. aeruginosa, and c-di-GMP is now recognized to regulate many important biological processes in pathogenesis. The c-di-GMP signalling mechanisms in P. aeruginosa have been studied extensively in the past decade, revealing complicated c-di-GMP metabolism and signalling network. In this review, the underlying mechanisms of this signalling network will be discussed, mainly focussing on how environmental cues regulate c-di-GMP signalling, protein-protein interaction mediated functional regulation, heterogeneity of c-di-GMP and cross talk between c-di-GMP signalling and other signalling systems. Understanding the molecular mechanism underlying the complex c-di-GMP signalling network would be beneficial for developing therapeutic approaches and antibacterial agents to combat the threat from P. aeruginosa.

Escherichia coli is one of the most notorious pathogens for its ability to adapt, colonize, and proliferate in different habitats through a multitude of acquired virulence factors. Its presence affects the food-processing industry and causes food poisoning, being also a major economic burden for the food, agriculture, and health sectors. Bacteriophages are emerging as an appealing strategy to mitigate bacterial pathogens, including specific E. coli pathovars, without exerting a deleterious effect on humans and animals. This review globally analyzes the applied research on E. coli phages for veterinary, food, and human use. It starts by describing the pathogenic E. coli pathotypes and their relevance in human and animal context. The idea that phages can be used as a One Health approach to control and interrupt the transmission routes of pathogenic E. coli is sustained through an exhaustive revision of the recent literature. The emerging phage formulations, genetic engineering and encapsulation technologies are also discussed as a means of improving phage-based control strategies, with a particular focus on E. coli pathogens.

Eggs contaminated with Salmonella have been internationally significant sources of human illness for several decades. Most egg-associated illness has been attributed to Salmonella serovar Enteritidis, but a few other serovars (notably S. Heidelberg and S. Typhimurium) are also sometimes implicated. The edible interior contents of eggs typically become contaminated with S. Enteritidis because the pathogen's unique virulence attributes enable it to colonize reproductive tissues in systemically infected laying hens. Other serovars are more commonly associated with surface contamination of eggshells. Both research and field experience have demonstrated that the most effective overall Salmonella control strategy in commercial laying flocks is the application of multiple interventions throughout the egg production cycle. At the preharvest (egg production) level, intervention options of demonstrated efficacy include vaccination and gastrointestinal colonization control via treatments such as prebiotics, probiotics, and bacteriophages, Effective environmental management of housing systems used for commercial laying flocks is also essential for minimizing opportunities for the introduction, transmission, and persistence of Salmonella in laying flocks. At the postharvest (egg processing and handling) level, careful regulation of egg storage temperatures is critical for limiting Salmonella multiplication inside the interior contents.

Integrative Conjugative Elements (ICEs) are mosaics containing functional modules allowing maintenance by site-specific integration and excision into and from the host genome and conjugative transfer to a specific host range. Many ICEs encode a range of adaptive functions that aid bacterial survival and evolution in a range of niches. ICEs from the SXT/R391 family are found in γ-Proteobacteria. Over 100 members have undergone epidemiological and molecular characterization allowing insight into their diversity and function. Comparative analysis of SXT/R391 elements from a wide geographic distribution has revealed conservation of key functions, and the accumulation and evolution of adaptive genes. This evolution is associated with gene acquisition in conserved hotspots and variable regions within the SXT/R391 ICEs catalysed via element-encoded recombinases. The elements can carry IS elements and transposons, and a mutagenic DNA polymerase, PolV, which are associated with their evolution. SXT/R391 ICEs isolated from different niches appear to have retained adaptive functions related to that specific niche; phage resistance determinants in ICEs carried by wastewater bacteria, antibiotic resistance determinants in clinical isolates and metal resistance determinants in bacteria recovered from polluted environments/ocean sediments. Many genes found in the element hotspots are undetermined and have few homologs in the nucleotide databases.

A stable but reversible phenotype switch from normal to persister state is advantageous to the intracellular pathogens to cause recurrent infections and to evade the host immune system. Staphylococcus aureus is a versatile opportunistic pathogen known to cause chronic infections with significant mortality. One of the notable features is the ability to switch to a per-sisters cell, which is found in planktonic and biofilm states. This phenotypic switch is always an open question to explore the hidden fundamental science that coheres with a calculated or fortuitous move. Toxin-antitoxin modules, nutrient stress, and an erroneous translation-enabled state of dormancy entail this persistent behaviour in S. aureus. It is paramount to get a clear picture of why the cell chooses to enter a persistent condition, as it would decide the course of treatment. Analyzing the exit from a persistent state to an active state and the subsequent repercussion of this transition is essential to determine its role in chronic infections. This review attempts to provide a constructed argument discussing the most widely accepted mechanisms and identifying the various attributes of persistence.